Schistosomiasis is a global disease that infects more than 207 million people worldwide. Treatment for schistosomiasis primarily relies on the drug, praziquantel, which has been in use for more than 30 years. Although praziquantel is available, over 250,000 people die each year from complications associated with schistosome infection, and there are few new anti-schistosome drugs undergoing active development. The schistosome genome has been sequenced, but a major hurdle for schistosome drug development has been the inability to efficiently manipulate schistosome genetically resulting in our limited understanding of schistosome molecular programs. Our long-term goals are to rationally identify potential drug targets for use against schistosomiasis. We plan to progress toward this goal by defining the regulatory programs required for schistosome development and viability. This process can be facilitated with tools that promote our ability to genetically modif and manipulate schistosome parasites. This study provides an alternative and new method for the transfection of nucleic acid in schistosomes to genetically control schistosome signaling systems through DNA overexpression, protein localization, and the utilization and the development of RNA interference strategies. It will simplify and improve current methods for transfection and will have a major impact on schistosome, and parasitic worm molecular genetics in general.